Do You Zoster Vaccinate? (6.19.2026) Save
Transcription
It's June 19, 2026. This is the RheumNow podcast. Hi, I'm Dr. Jack Cush, executive editor of RheumNow.com. This week, some big questions on the podcast. Should you be prescribing glucosamine? Should you be talking to your interventional radiologist about treatment of knee OA? Should you be using oral or subq methotrexate? These are kind of important questions, right?
Let's begin with a report from scientific advances. This was an interesting study potentially about the pathogenesis of Sjögren's disease where this report showed how Ro60 antibodies, as you know, when you do SSA or Ro testing, you're really testing for Ro52 and Ro60. Ro52 is the big one. Usually you're testing for both, but this particular report in Science was about Ro60 as a driver of CD4-specific T-cell responses to Ro60 that led to Ro60-specific B cell hyperactivity and humoral activity, basically saying Ro60 is a driver of disease. And I thought it was interesting, which led me to look into Ro52 versus Ro60, and the bottom line is 70% of people with Sjögren's are SSA or Ro positive, and that most of that probably is Ro52. I think the number is — well, first, 30% of people are seronegative for Ro and La, and people who are Ro positive by 52 or 60 are going to have usually more active disease. Seronegatives tend to have milder disease — just dry eyes, dry mouth, and not much more, and mild at that. But it turns out that about 50% of people with Sjögren's disease are double positive for antibodies against Ro52 and Ro60, and that about 10 to 20% are only Ro60, but Ro60 positivity only seems to correlate with milder disease, not major organ disease, not the really scary stuff in Sjögren's. Nonetheless, this report says there is a Ro60-specific T and B cell orchestrated response that could contribute to the pathogenesis of the disease. I think we'll be seeing obviously a lot more Sjögren's research and pathogenesis studies as we get into more studies for Sjögren's. I hope that we'll see that.
Another study I saw this week that kind of got my attention was GI involvement in patients with dermatomyositis. I don't usually think of dermatomyositis having much in the way of GI involvement. Well, yes — you know, 50% of people may have dysphagia because it's the upper third of the esophagus, the skeletal muscle disease — why not dysphagia? But they can have more than that. The prevalence of GI involvement in dermatomyositis was assessed in two different cohorts of 167 patients. Overall, up to 50% of patients can have that, but severe GI involvement is seen mainly in NXP2 antibody-positive patients, much more so than MDA5 or any of the other subgroups of dermatomyositis. So much so that NXP2 has an 8.8-fold higher risk of severe GI involvement. Those who are NXP2 positive and had severe GI disease tend to be younger, with facial edema at presentation, with — as you would expect — both active skin and muscle disease. It seems like a unique subset. It seems to be uniquely associated with NXP2, and as you know, long ago I never did a lot of myositis-specific autoantibody testing. I wasn't sure about it. Now I'm doing more of it. I do think that there's something to NXP2 — as we know, it's got an association with calcinosis, right? MDA5 is a bad player. So I think doing that testing is a good idea.
An article from Radiology hit on a subject that I think is interesting, that led me to do a little more research, and that is genicular artery embolization. We've reported on this two or three times. It looks like it's an alternative treatment for people with problematic knee OA. Basically, you use something that embolizes that artery, it produces a pain benefit. And so this particular study from Radiology, not surprisingly — I think it was 200 patients — showed a clear-cut benefit. But then I looked at this, you know, I went to Open Evidence, I did a PubMed search, and you know what the bottom line is? Studies like this — open-label, single-center designs where there isn't a control group or a comparison — or meta-analyses basically say that genicular artery embolization is clearly beneficial with regard to pain and should be considered. Wait a second, there's more. There are actually three sham placebo-controlled trials that show no significant benefit. So the story is out on whether you should be doing this. You know, you talk to the radiologist — let's say, yeah, we should do that, and we should do radiation for knee OA — and that's a special kind of stupid. I would not endorse this. And to back that up, so far — not that the guidelines are up to date, ACR OA treatment guidelines, I think we are 5 years overdue — but the ACR and EULAR guidelines on OA treatment do not mention the utility of GAE, genicular artery embolization. And there are some issues about the substance you use to embolize and cut off that arterial supply. This needs to go to the drawing board. We need more information before
we start doing this. Nature published something interesting that pertains to Alzheimer's, something you don't want to deal with. Um, and glucosamine, something you probably don't endorse. But there's an article uh fairly well done showing that amongst the many mechanisms that drive Alzheimer's disease, one of it is hyper glycosylation, which you know if you read about it, it's kind of interesting and whatnot, but um it turns out that glucosamine um increases hyper glycosylation. Glucosamine is taken by about 7% of elderly people over age 70, presumably it's for arthritis prevention or arthritis management. It's as you know from the study that I did in New England Journal that glucosamine doesn't really work. Um not much better than placebo. Uh and you could argue about whether it's got utility or not. I don't think it does. Um in this paper they did mention a retrospective uh electronic health record study showed that um uh in Alzheimer's patients the use of glucosamine has been associated with progression of Alzheimer's disease or worse survival in Alzheimer's disease. So, if you're worried about Alzheimer's, make sure they're not taking glucosamine because there is no positive data and again, it doesn't seem to produce any articular benefit that I can point to.
Uh, a report a month or two before EULAR came out um looked at uh what happens when you treat undifferentiated early arthritis. So these don't meet criteria for clinically suspect arthritis or preclinical RA because they don't have to be uh rheumatoid factor or CCP positive. So in this particular study these were um undifferentiated arthritis who had two or more um swollen joints but didn't meet criteria for RA and they looked at um — they enrolled patients and treated them either with non-steroidals or methotrexate starting out at 15 going up to 25 or baricitinib 4 milligrams a day, about 28 patients in each group. These people had really mild disease at entry. Their DAS scores were 2.8. They had two or three swollen joints. Uh less than 17% were CCP positive.
At 3 months, baricitinib was better than non-steroidals or methotrexate, which were equivalent in their response rates. And so baricitinib lowered the DAS-28 score from 2.4 down to what looks like about 1.9, a drop of minus 0.52 in DAS points, and that was significant at 3 months. However, when you follow those people out to 12 months, they all did better. They all got their DAS scores down to less than 1.7. But the best at 12 months was um methotrexate at 1.3, non-steroidal at 1.6, and baricitinib at 1.7. So baricitinib had the fastest response but it didn't go much beyond what it achieved at 3 months when you looked out at 12 months.
This is a small study. Um I don't think this is an endorsement of treating undifferentiated arthritis. But you know the bottom line is someone who has a chronic arthropathy of more than 12 weeks of a swollen joint needs to be treated and needs to be treated with a DMARD. What you call them um can then refer to what the success of therapy may be. If they are clinically suspect arthralgia where they shouldn't have two or three swollen joints, right? But they are seropositive, we really don't know what to do. You might do abatacept, but in these undifferentiated uh arthritis polyarthritis patients with two or three swollen joints, DMARDs — you know it looks like that all these were good choices but maybe the best choice was methotrexate, um with non-steroidal and baricitinib doing about the same.
Interesting — uh a study looked at elderly um RA patients um between 2009 and 2022. So they did a 20% sampling of elderly Medicare patients over the age of 65 who were on TNF inhibitors and found the ones who either stopped or tapered their TNF inhibitor. So the cohort was 949 patients and they found that um only 38% of them were able to de-escalate TNF inhibitor therapy — either stop it or lower the dose. Um but that 62% had to re-escalate the therapy. So if you want to withdraw therapy, it's only going to be effective 38% of the time in your elderly RA patients. Re-escalation was more likely in 60% or more of patients and um it took 160 days for them to re-escalate. So it wasn't like an immediate flare of activity. Re-escalation was more likely in people who were Black, Hispanic, non-white with a lower comorbidity burden. I don't know that that helps me but maybe it helps you and that's why I reported it.
Um the question next uh in this next report is what's happening with steroid doses in newly diagnosed RA. You know the clinical trials say — I'm not even going to look at this report and say the clinical trials say that people who are bad enough to get into clinical trials, about 60% — 50, 60% — are taking corticosteroids. You know usually a dose that's a little above 5 milligrams per day and that doesn't change in clinical trials. Right? So this study um was a Danish uh single center hospital. 574 newly diagnosed RA patients. 75% went on
to receive steroids in some form in their first year. 55% received it at their first visit. The mean dose was 9.3 milligrams per day. Half the patients who received steroids were receiving oral steroids. 47% received intraarticular steroids. 20% had an infection in the first year with a 13% increased risk. But the confidence intervals overlap one, saying that this was not a significant increase in infections when you looked at steroid exposure, but it tended that way. But the numbers here may not be large enough. Other studies have shown that at this dose, you know, 5 to 10 milligrams, there is an increased risk of serious infections. So anyway, I think we're still using steroids. I think we're still using too much steroids and we do know steroids are bad for you in RA and other inflammatory arthropathies.
As you may have remembered during COVID, I was all gung-ho and wild about the use of telemedicine by rheumatologists. In the first year after COVID, rheumatologists were the second leading group using telemedicine successfully, but since COVID has died so has your interest in telemedicine. Only a minority of you are doing this. So this report about a recent US telehealth utilization showed it increased 10% in the first quarter of 2026. It went up from overall medical claims from 5% to 5.5%. Who's using telemedicine the most out there right now? It still is mental health, which makes up more than half of the use, which is gigantic compared to rheumatologists who are only using this in 3% of your visits for rheumatology. 3% overall — that number is a little higher in the western states, a little higher in the northeast. Telehealth overall, not in rheumatology, is being used in almost 60% for outpatient visits, 7% for new visits, and 35% for psychotherapy services, but again most of this use is in psychiatry and psychotherapy.
Why are you not doing telehealth? I saw a recent report from — I don't know if it was Deloitte or Becker's, one of these large companies that looks at healthcare in the United States — a great report about practice. A CEO of a big group in New Jersey said that the way that they manage urgent patient appointments is they built into their system a telehealth arm, and someone assigned to telehealth every day is the one who communicates with people who need to be seen today, an hour from now, and they're always available. And when they're not doing telehealth they're out there doing some other productive work, but everybody has their rotation and everybody then who calls and needs to be seen by someone right away is seen by Dr. Mo, Dr. Sarah, Dr. Ellen, whoever. They manage the problem as opposed to trying to manage it over the phone, which is dangerous, and then make an appropriate follow-up.
I still think we should be doing more telehealth because you can do it in rheumatology where other specialties can't. And if you don't think you can, look at my video on the virtual joint exam. It's very accurate. I'm really good at telehealth.
A study on polychondritis — relapsing polychondritis — proves that I'm not very good at that because I don't see very much of that. A study coming out of Kyoto University looked at 55 patients with relapsing polychondritis followed for a total of 500 patient years, almost 10 years follow-up. And they looked at how they responded to different treatments. So they either received a TNF inhibitor, an IL-6 inhibitor, or no biologic. The relapse rates were highest with, as you might guess, no biologic — 47 per 100 patient years, meaning a relapsing polychondritis patient, 100 of them followed for one year, half of them were going to have a flare. The relapse rates for the biologics was substantially less: 22 per 100 patient years with a TNF inhibitor and even lower, 12.5 per 100 patient years with an IL-6 inhibitor. Now again, this comes from Japan where they're IL-6 happy and they have the most amount of experience. Would that be something you see in your practice? I think you would. So again, TNF inhibitors lower the risk by 60%. The IL-6 inhibitors lower the risk by 80%. This study was unable to comment about biologic use and risk of infections — the numbers were too imprecise to make a comment, is what they said.
I don't know if you get the email that I send out every Saturday morning on the RheumNow IQ quiz. It's been wildly successful with you and many of your colleagues. The one that went out after EULAR had a lot more questions — 30 in the first week and 15 in the second week. In last week's survey, only half of you got this question right. This question being: in macrophage activation syndrome and treatment of it, which cytokine is a central target of the FDA-approved drug emapalumab for MAS and MAS associated with Still's? Emapalumab — we've covered it here before — it's an anti-gamma interferon monoclonal antibody, highly successful, but only half of you got that right. Look at your inbox on
Saturday morning RheumNow IQ coming your way. A report from the Medical College of Wisconsin — Mishod and colleagues looked at vaccination in people on JAK inhibitors. Single center study, 102 patients treated with a JAK inhibitor, 72% were over the age of 50, 77% were RA patients. Showed that of this 102 — and again at least 70% are eligible by age — only 27% received at least one dose of the recombinant zoster vaccine, also known as Shingrix. What's the deal? And only three — I'm going to say is that so it's 3% or three patients — received the vaccine within 30 days of the JAK inhibitor.
What's going on here folks? You know the data is really clear. I'm going to talk about vaccination recommendations at the end of this where they say everybody on immunosuppression should get the Shingrix vaccine. But I put anybody on a JAK inhibitor — I put them, I give them the Shingrix vaccine. I like to get it before. It doesn't have to be before. They need to get at least one dose, but two doses are better. And I'll give it at any age. It works.
Again, going on a JAK inhibitor or inhibitor of an alpha interferon like anifrolumab is a gigantic increase over any of the other biologics and over just active RA or elderly RA. Right? The population risk of zoster is 6 to 10 per thousand. On a TNF inhibitor, it's like 12 to 15 per thousand. On a JAK inhibitor, it's like 45 per thousand. It really goes up a lot. I vaccinate everybody with the recombinant zoster vaccine who goes on a JAK inhibitor. Maybe you don't. Tell me why.
So here are the recommendations that came out of EULAR. This was a publication this week that you should look over. It's a nice, I think, quick look. The bottom line is that there were, I think, five overarching statements and 10 guideline recommendations on different vaccines.
Number one, they were very proactive about us in rheumatology using vaccines, having a plan for the vaccines as soon as you diagnose a patient, using them as soon as possible. And by the way, you should be vaccinating people independent of disease activity — as you know it's, you really do — it's not independent of drugs, because rituximab and methotrexate really impair vaccine responses, so you need a strategy for those. But independent of disease activity, non-live vaccines can be given at any time, any situation, and don't worry about it.
Live attenuated vaccines, as the package insert says, should be not just avoided, but now these guidelines say they can be considered with caution, because there are instances where a live attenuated vaccine could be used, like in the case of yellow fever. Flu — they say give the flu vaccine, hold methotrexate for one week. Any of the pneumococcal vaccines — you know, the Prevnar 20, the Prevnar 13 — you should, based on the VACCINATE study which we covered a few weeks ago, hold the methotrexate for 4 weeks. And in both those instances, with flu and with the pneumococcal vaccines, there's not a flare of RA activity by holding the methotrexate.
They say that the Shingrix vaccine is strongly recommended for patients with autoimmune and inflammatory rheumatic disease on immunosuppressive therapy. Immunogenicity is relatively well preserved — that's humoral responses — in people on JAK inhibitors; however, cellular responses are attenuated and further reduced in people also on methotrexate. So you need a rule for methotrexate that applies when you're giving the Shingrix — maybe you should hold the methotrexate for a week like you do with the flu or the pneumococcal — but there's no study to prove that.
Newborns should not get live vaccines, especially if the mother has been exposed to biologic DMARDs and hence the fetus would have been exposed. But it is safe to give the rotavirus vaccine in the first six months in mothers who had antenatal TNF exposure. And they are very strong in saying everyone — our patients — should be receiving the COVID vaccine.
Another recommendation guideline coming out of EULAR 2026 — both of these presented on the last day of EULAR. This was the recommendations for the treatment of PMR, GCA, and Takayasu's. PMR and GCA go together. GCA is large vessel vasculitis. I guess they threw in the other large vessel vasculitis because there's really only one big one — that's Takayasu's. Well, it's kind of an awkward grouping if you ask me.
The bottom line here is that they say a few things you should pay attention to. One, glucocorticoid treatment in these three diseases can be delayed until diagnosis is confirmed — however, not with giant cell arteritis, meaning there's urgency and you need to start steroids right away. The other thing is response to glucocorticoids is not a diagnostic test for any of these disorders, and that's something that people often talk about with new onset PMR. The starting dose is 15 to 25 milligrams. That should be tapered to 10 milligrams within 1 to 2 months, with the aim of stopping within one year.
Good luck with that. Everyone talks a good game, but the reality is we're not so good at getting people off steroids. In relapsing or refractory PMR, sarilumab is preferred. Tocilizumab is an alternative. And they say if you must, you can use methotrexate. Although I asked the author this, the data sucks for methotrexate. They said they included it in the guidelines because these biologics are not always available in every country. And oh, by the way, we rheumatologists are familiar with methotrexate. So why not? Well, the data is pretty mixed on methotrexate. It's up to you whether you use it. You can say the same thing for GCA.
In GCA, again, urgent referral is necessary. Urgent treatment with glucocorticoids has to be done immediately without waiting for confirmatory investigations, because it is a medical emergency.
One more thing about PMR — they say that refractory PMR should make you — and I've never thought this way — should make you think about a re-evaluation of the diagnosis. Maybe it's not PMR, because PMR mimics could include myositis, inflammatory arthritis, paraneoplastic presentations, myeloma, etc. That's something that seems really smart.
So again, GCA is urgent, a medical emergency. Do the things you have to do. Start steroids right away. New onset GCA gets 40 to 60 milligrams a day tapered to 15 or 20 within 3 months, with the aim to stop glucocorticoids within 18 months. Relapses should be treated as new onset disease. Minor relapses — you can escalate to your last effective steroid dose. Steroid sparing can be accomplished with tocilizumab or mavrilimumab, especially in those people who are refractory or relapsing, instead of using more and more steroids. They also say here methotrexate is an alternative — not in my clinic, but maybe in yours.
And they did talk in both GCA and Takayasu's about vascular complications requiring specialized urgent referral to vascular surgeons for management of the problem — that if there's going to be a vascular intervention for a dissection or critical ischemia, it should be done during periods of stable remission rather than when the patient's wickedly inflammatory. But sometimes you can't do that. Again, interventions carry risks here, and you want to do the endovascular interventions to lower risks without incurring new risks. But the guidelines are really good at spelling this out. You might want to look at that report.
I would encourage you, if you aren't well versed in what happened at EULAR 2025, many of us were there. I'm going to give you three ways — and they'll be in the show notes for this that you can click and do this. The first way and the easy way is a 55-minute recording called the EULAR RheumNow Roundup with Artie Kavanaugh and I talking about, I think, 16 or 17 of our favorite presentations. You'll get a good taste in one hour — that's one or two car rides or one sit-down. You can look at the video, you can listen to the podcast.
The next best, which I think is really valuable, is listening to the topic panels. We have three topic panels. Usually we have four or five during ACR, but for EULAR we only had enough staff to do three. We have a topic panel on RA, on PsA, and on CAR T cell therapies, where four of us get together and talk about eight of the most important abstracts in that particular topic. I think you'd get a really good overview on either RA, PsA, or CAR T cell if you looked at one of those.
And the other way, which I really like and is very very popular — both these topic panels and daily recaps got tons of podcast listens and many hundreds of video views — the daily recaps: we did a combined day one/day two recap, and then a day three and a day four recap. So there are three recaps, either as videos or podcasts that you can listen to. Each of these topic panels and daily recaps are about 30 minutes long and have four people. We're going over about eight abstracts, some of the favorite things that fit for that day. So the daily recaps are different than the topic panels because it's like the best thing I saw today from the four people who were on that particular video panel that we did. They go fast, they're interesting. I hope you enjoy them. Tune in next week for more on RheumNow.
Let's begin with a report from scientific advances. This was an interesting study potentially about the pathogenesis of Sjögren's disease where this report showed how Ro60 antibodies, as you know, when you do SSA or Ro testing, you're really testing for Ro52 and Ro60. Ro52 is the big one. Usually you're testing for both, but this particular report in Science was about Ro60 as a driver of CD4-specific T-cell responses to Ro60 that led to Ro60-specific B cell hyperactivity and humoral activity, basically saying Ro60 is a driver of disease. And I thought it was interesting, which led me to look into Ro52 versus Ro60, and the bottom line is 70% of people with Sjögren's are SSA or Ro positive, and that most of that probably is Ro52. I think the number is — well, first, 30% of people are seronegative for Ro and La, and people who are Ro positive by 52 or 60 are going to have usually more active disease. Seronegatives tend to have milder disease — just dry eyes, dry mouth, and not much more, and mild at that. But it turns out that about 50% of people with Sjögren's disease are double positive for antibodies against Ro52 and Ro60, and that about 10 to 20% are only Ro60, but Ro60 positivity only seems to correlate with milder disease, not major organ disease, not the really scary stuff in Sjögren's. Nonetheless, this report says there is a Ro60-specific T and B cell orchestrated response that could contribute to the pathogenesis of the disease. I think we'll be seeing obviously a lot more Sjögren's research and pathogenesis studies as we get into more studies for Sjögren's. I hope that we'll see that.
Another study I saw this week that kind of got my attention was GI involvement in patients with dermatomyositis. I don't usually think of dermatomyositis having much in the way of GI involvement. Well, yes — you know, 50% of people may have dysphagia because it's the upper third of the esophagus, the skeletal muscle disease — why not dysphagia? But they can have more than that. The prevalence of GI involvement in dermatomyositis was assessed in two different cohorts of 167 patients. Overall, up to 50% of patients can have that, but severe GI involvement is seen mainly in NXP2 antibody-positive patients, much more so than MDA5 or any of the other subgroups of dermatomyositis. So much so that NXP2 has an 8.8-fold higher risk of severe GI involvement. Those who are NXP2 positive and had severe GI disease tend to be younger, with facial edema at presentation, with — as you would expect — both active skin and muscle disease. It seems like a unique subset. It seems to be uniquely associated with NXP2, and as you know, long ago I never did a lot of myositis-specific autoantibody testing. I wasn't sure about it. Now I'm doing more of it. I do think that there's something to NXP2 — as we know, it's got an association with calcinosis, right? MDA5 is a bad player. So I think doing that testing is a good idea.
An article from Radiology hit on a subject that I think is interesting, that led me to do a little more research, and that is genicular artery embolization. We've reported on this two or three times. It looks like it's an alternative treatment for people with problematic knee OA. Basically, you use something that embolizes that artery, it produces a pain benefit. And so this particular study from Radiology, not surprisingly — I think it was 200 patients — showed a clear-cut benefit. But then I looked at this, you know, I went to Open Evidence, I did a PubMed search, and you know what the bottom line is? Studies like this — open-label, single-center designs where there isn't a control group or a comparison — or meta-analyses basically say that genicular artery embolization is clearly beneficial with regard to pain and should be considered. Wait a second, there's more. There are actually three sham placebo-controlled trials that show no significant benefit. So the story is out on whether you should be doing this. You know, you talk to the radiologist — let's say, yeah, we should do that, and we should do radiation for knee OA — and that's a special kind of stupid. I would not endorse this. And to back that up, so far — not that the guidelines are up to date, ACR OA treatment guidelines, I think we are 5 years overdue — but the ACR and EULAR guidelines on OA treatment do not mention the utility of GAE, genicular artery embolization. And there are some issues about the substance you use to embolize and cut off that arterial supply. This needs to go to the drawing board. We need more information before
we start doing this. Nature published something interesting that pertains to Alzheimer's, something you don't want to deal with. Um, and glucosamine, something you probably don't endorse. But there's an article uh fairly well done showing that amongst the many mechanisms that drive Alzheimer's disease, one of it is hyper glycosylation, which you know if you read about it, it's kind of interesting and whatnot, but um it turns out that glucosamine um increases hyper glycosylation. Glucosamine is taken by about 7% of elderly people over age 70, presumably it's for arthritis prevention or arthritis management. It's as you know from the study that I did in New England Journal that glucosamine doesn't really work. Um not much better than placebo. Uh and you could argue about whether it's got utility or not. I don't think it does. Um in this paper they did mention a retrospective uh electronic health record study showed that um uh in Alzheimer's patients the use of glucosamine has been associated with progression of Alzheimer's disease or worse survival in Alzheimer's disease. So, if you're worried about Alzheimer's, make sure they're not taking glucosamine because there is no positive data and again, it doesn't seem to produce any articular benefit that I can point to.
Uh, a report a month or two before EULAR came out um looked at uh what happens when you treat undifferentiated early arthritis. So these don't meet criteria for clinically suspect arthritis or preclinical RA because they don't have to be uh rheumatoid factor or CCP positive. So in this particular study these were um undifferentiated arthritis who had two or more um swollen joints but didn't meet criteria for RA and they looked at um — they enrolled patients and treated them either with non-steroidals or methotrexate starting out at 15 going up to 25 or baricitinib 4 milligrams a day, about 28 patients in each group. These people had really mild disease at entry. Their DAS scores were 2.8. They had two or three swollen joints. Uh less than 17% were CCP positive.
At 3 months, baricitinib was better than non-steroidals or methotrexate, which were equivalent in their response rates. And so baricitinib lowered the DAS-28 score from 2.4 down to what looks like about 1.9, a drop of minus 0.52 in DAS points, and that was significant at 3 months. However, when you follow those people out to 12 months, they all did better. They all got their DAS scores down to less than 1.7. But the best at 12 months was um methotrexate at 1.3, non-steroidal at 1.6, and baricitinib at 1.7. So baricitinib had the fastest response but it didn't go much beyond what it achieved at 3 months when you looked out at 12 months.
This is a small study. Um I don't think this is an endorsement of treating undifferentiated arthritis. But you know the bottom line is someone who has a chronic arthropathy of more than 12 weeks of a swollen joint needs to be treated and needs to be treated with a DMARD. What you call them um can then refer to what the success of therapy may be. If they are clinically suspect arthralgia where they shouldn't have two or three swollen joints, right? But they are seropositive, we really don't know what to do. You might do abatacept, but in these undifferentiated uh arthritis polyarthritis patients with two or three swollen joints, DMARDs — you know it looks like that all these were good choices but maybe the best choice was methotrexate, um with non-steroidal and baricitinib doing about the same.
Interesting — uh a study looked at elderly um RA patients um between 2009 and 2022. So they did a 20% sampling of elderly Medicare patients over the age of 65 who were on TNF inhibitors and found the ones who either stopped or tapered their TNF inhibitor. So the cohort was 949 patients and they found that um only 38% of them were able to de-escalate TNF inhibitor therapy — either stop it or lower the dose. Um but that 62% had to re-escalate the therapy. So if you want to withdraw therapy, it's only going to be effective 38% of the time in your elderly RA patients. Re-escalation was more likely in 60% or more of patients and um it took 160 days for them to re-escalate. So it wasn't like an immediate flare of activity. Re-escalation was more likely in people who were Black, Hispanic, non-white with a lower comorbidity burden. I don't know that that helps me but maybe it helps you and that's why I reported it.
Um the question next uh in this next report is what's happening with steroid doses in newly diagnosed RA. You know the clinical trials say — I'm not even going to look at this report and say the clinical trials say that people who are bad enough to get into clinical trials, about 60% — 50, 60% — are taking corticosteroids. You know usually a dose that's a little above 5 milligrams per day and that doesn't change in clinical trials. Right? So this study um was a Danish uh single center hospital. 574 newly diagnosed RA patients. 75% went on
to receive steroids in some form in their first year. 55% received it at their first visit. The mean dose was 9.3 milligrams per day. Half the patients who received steroids were receiving oral steroids. 47% received intraarticular steroids. 20% had an infection in the first year with a 13% increased risk. But the confidence intervals overlap one, saying that this was not a significant increase in infections when you looked at steroid exposure, but it tended that way. But the numbers here may not be large enough. Other studies have shown that at this dose, you know, 5 to 10 milligrams, there is an increased risk of serious infections. So anyway, I think we're still using steroids. I think we're still using too much steroids and we do know steroids are bad for you in RA and other inflammatory arthropathies.
As you may have remembered during COVID, I was all gung-ho and wild about the use of telemedicine by rheumatologists. In the first year after COVID, rheumatologists were the second leading group using telemedicine successfully, but since COVID has died so has your interest in telemedicine. Only a minority of you are doing this. So this report about a recent US telehealth utilization showed it increased 10% in the first quarter of 2026. It went up from overall medical claims from 5% to 5.5%. Who's using telemedicine the most out there right now? It still is mental health, which makes up more than half of the use, which is gigantic compared to rheumatologists who are only using this in 3% of your visits for rheumatology. 3% overall — that number is a little higher in the western states, a little higher in the northeast. Telehealth overall, not in rheumatology, is being used in almost 60% for outpatient visits, 7% for new visits, and 35% for psychotherapy services, but again most of this use is in psychiatry and psychotherapy.
Why are you not doing telehealth? I saw a recent report from — I don't know if it was Deloitte or Becker's, one of these large companies that looks at healthcare in the United States — a great report about practice. A CEO of a big group in New Jersey said that the way that they manage urgent patient appointments is they built into their system a telehealth arm, and someone assigned to telehealth every day is the one who communicates with people who need to be seen today, an hour from now, and they're always available. And when they're not doing telehealth they're out there doing some other productive work, but everybody has their rotation and everybody then who calls and needs to be seen by someone right away is seen by Dr. Mo, Dr. Sarah, Dr. Ellen, whoever. They manage the problem as opposed to trying to manage it over the phone, which is dangerous, and then make an appropriate follow-up.
I still think we should be doing more telehealth because you can do it in rheumatology where other specialties can't. And if you don't think you can, look at my video on the virtual joint exam. It's very accurate. I'm really good at telehealth.
A study on polychondritis — relapsing polychondritis — proves that I'm not very good at that because I don't see very much of that. A study coming out of Kyoto University looked at 55 patients with relapsing polychondritis followed for a total of 500 patient years, almost 10 years follow-up. And they looked at how they responded to different treatments. So they either received a TNF inhibitor, an IL-6 inhibitor, or no biologic. The relapse rates were highest with, as you might guess, no biologic — 47 per 100 patient years, meaning a relapsing polychondritis patient, 100 of them followed for one year, half of them were going to have a flare. The relapse rates for the biologics was substantially less: 22 per 100 patient years with a TNF inhibitor and even lower, 12.5 per 100 patient years with an IL-6 inhibitor. Now again, this comes from Japan where they're IL-6 happy and they have the most amount of experience. Would that be something you see in your practice? I think you would. So again, TNF inhibitors lower the risk by 60%. The IL-6 inhibitors lower the risk by 80%. This study was unable to comment about biologic use and risk of infections — the numbers were too imprecise to make a comment, is what they said.
I don't know if you get the email that I send out every Saturday morning on the RheumNow IQ quiz. It's been wildly successful with you and many of your colleagues. The one that went out after EULAR had a lot more questions — 30 in the first week and 15 in the second week. In last week's survey, only half of you got this question right. This question being: in macrophage activation syndrome and treatment of it, which cytokine is a central target of the FDA-approved drug emapalumab for MAS and MAS associated with Still's? Emapalumab — we've covered it here before — it's an anti-gamma interferon monoclonal antibody, highly successful, but only half of you got that right. Look at your inbox on
Saturday morning RheumNow IQ coming your way. A report from the Medical College of Wisconsin — Mishod and colleagues looked at vaccination in people on JAK inhibitors. Single center study, 102 patients treated with a JAK inhibitor, 72% were over the age of 50, 77% were RA patients. Showed that of this 102 — and again at least 70% are eligible by age — only 27% received at least one dose of the recombinant zoster vaccine, also known as Shingrix. What's the deal? And only three — I'm going to say is that so it's 3% or three patients — received the vaccine within 30 days of the JAK inhibitor.
What's going on here folks? You know the data is really clear. I'm going to talk about vaccination recommendations at the end of this where they say everybody on immunosuppression should get the Shingrix vaccine. But I put anybody on a JAK inhibitor — I put them, I give them the Shingrix vaccine. I like to get it before. It doesn't have to be before. They need to get at least one dose, but two doses are better. And I'll give it at any age. It works.
Again, going on a JAK inhibitor or inhibitor of an alpha interferon like anifrolumab is a gigantic increase over any of the other biologics and over just active RA or elderly RA. Right? The population risk of zoster is 6 to 10 per thousand. On a TNF inhibitor, it's like 12 to 15 per thousand. On a JAK inhibitor, it's like 45 per thousand. It really goes up a lot. I vaccinate everybody with the recombinant zoster vaccine who goes on a JAK inhibitor. Maybe you don't. Tell me why.
So here are the recommendations that came out of EULAR. This was a publication this week that you should look over. It's a nice, I think, quick look. The bottom line is that there were, I think, five overarching statements and 10 guideline recommendations on different vaccines.
Number one, they were very proactive about us in rheumatology using vaccines, having a plan for the vaccines as soon as you diagnose a patient, using them as soon as possible. And by the way, you should be vaccinating people independent of disease activity — as you know it's, you really do — it's not independent of drugs, because rituximab and methotrexate really impair vaccine responses, so you need a strategy for those. But independent of disease activity, non-live vaccines can be given at any time, any situation, and don't worry about it.
Live attenuated vaccines, as the package insert says, should be not just avoided, but now these guidelines say they can be considered with caution, because there are instances where a live attenuated vaccine could be used, like in the case of yellow fever. Flu — they say give the flu vaccine, hold methotrexate for one week. Any of the pneumococcal vaccines — you know, the Prevnar 20, the Prevnar 13 — you should, based on the VACCINATE study which we covered a few weeks ago, hold the methotrexate for 4 weeks. And in both those instances, with flu and with the pneumococcal vaccines, there's not a flare of RA activity by holding the methotrexate.
They say that the Shingrix vaccine is strongly recommended for patients with autoimmune and inflammatory rheumatic disease on immunosuppressive therapy. Immunogenicity is relatively well preserved — that's humoral responses — in people on JAK inhibitors; however, cellular responses are attenuated and further reduced in people also on methotrexate. So you need a rule for methotrexate that applies when you're giving the Shingrix — maybe you should hold the methotrexate for a week like you do with the flu or the pneumococcal — but there's no study to prove that.
Newborns should not get live vaccines, especially if the mother has been exposed to biologic DMARDs and hence the fetus would have been exposed. But it is safe to give the rotavirus vaccine in the first six months in mothers who had antenatal TNF exposure. And they are very strong in saying everyone — our patients — should be receiving the COVID vaccine.
Another recommendation guideline coming out of EULAR 2026 — both of these presented on the last day of EULAR. This was the recommendations for the treatment of PMR, GCA, and Takayasu's. PMR and GCA go together. GCA is large vessel vasculitis. I guess they threw in the other large vessel vasculitis because there's really only one big one — that's Takayasu's. Well, it's kind of an awkward grouping if you ask me.
The bottom line here is that they say a few things you should pay attention to. One, glucocorticoid treatment in these three diseases can be delayed until diagnosis is confirmed — however, not with giant cell arteritis, meaning there's urgency and you need to start steroids right away. The other thing is response to glucocorticoids is not a diagnostic test for any of these disorders, and that's something that people often talk about with new onset PMR. The starting dose is 15 to 25 milligrams. That should be tapered to 10 milligrams within 1 to 2 months, with the aim of stopping within one year.
Good luck with that. Everyone talks a good game, but the reality is we're not so good at getting people off steroids. In relapsing or refractory PMR, sarilumab is preferred. Tocilizumab is an alternative. And they say if you must, you can use methotrexate. Although I asked the author this, the data sucks for methotrexate. They said they included it in the guidelines because these biologics are not always available in every country. And oh, by the way, we rheumatologists are familiar with methotrexate. So why not? Well, the data is pretty mixed on methotrexate. It's up to you whether you use it. You can say the same thing for GCA.
In GCA, again, urgent referral is necessary. Urgent treatment with glucocorticoids has to be done immediately without waiting for confirmatory investigations, because it is a medical emergency.
One more thing about PMR — they say that refractory PMR should make you — and I've never thought this way — should make you think about a re-evaluation of the diagnosis. Maybe it's not PMR, because PMR mimics could include myositis, inflammatory arthritis, paraneoplastic presentations, myeloma, etc. That's something that seems really smart.
So again, GCA is urgent, a medical emergency. Do the things you have to do. Start steroids right away. New onset GCA gets 40 to 60 milligrams a day tapered to 15 or 20 within 3 months, with the aim to stop glucocorticoids within 18 months. Relapses should be treated as new onset disease. Minor relapses — you can escalate to your last effective steroid dose. Steroid sparing can be accomplished with tocilizumab or mavrilimumab, especially in those people who are refractory or relapsing, instead of using more and more steroids. They also say here methotrexate is an alternative — not in my clinic, but maybe in yours.
And they did talk in both GCA and Takayasu's about vascular complications requiring specialized urgent referral to vascular surgeons for management of the problem — that if there's going to be a vascular intervention for a dissection or critical ischemia, it should be done during periods of stable remission rather than when the patient's wickedly inflammatory. But sometimes you can't do that. Again, interventions carry risks here, and you want to do the endovascular interventions to lower risks without incurring new risks. But the guidelines are really good at spelling this out. You might want to look at that report.
I would encourage you, if you aren't well versed in what happened at EULAR 2025, many of us were there. I'm going to give you three ways — and they'll be in the show notes for this that you can click and do this. The first way and the easy way is a 55-minute recording called the EULAR RheumNow Roundup with Artie Kavanaugh and I talking about, I think, 16 or 17 of our favorite presentations. You'll get a good taste in one hour — that's one or two car rides or one sit-down. You can look at the video, you can listen to the podcast.
The next best, which I think is really valuable, is listening to the topic panels. We have three topic panels. Usually we have four or five during ACR, but for EULAR we only had enough staff to do three. We have a topic panel on RA, on PsA, and on CAR T cell therapies, where four of us get together and talk about eight of the most important abstracts in that particular topic. I think you'd get a really good overview on either RA, PsA, or CAR T cell if you looked at one of those.
And the other way, which I really like and is very very popular — both these topic panels and daily recaps got tons of podcast listens and many hundreds of video views — the daily recaps: we did a combined day one/day two recap, and then a day three and a day four recap. So there are three recaps, either as videos or podcasts that you can listen to. Each of these topic panels and daily recaps are about 30 minutes long and have four people. We're going over about eight abstracts, some of the favorite things that fit for that day. So the daily recaps are different than the topic panels because it's like the best thing I saw today from the four people who were on that particular video panel that we did. They go fast, they're interesting. I hope you enjoy them. Tune in next week for more on RheumNow.
If you are a health practitioner, you may Login/Register to comment.
Due to the nature of these comment forums, only health practitioners are allowed to comment at this time.